[Cited FineTest ELISA Kit] Current Research on Colorectal Cancer Therapy

FineTest ELISA kit contributes to the research on colorectal cancer therapy. The immunoassay is designed to measure IL-10 level in serum.

Article Title: Interleukin-10 deficiency suppresses colorectal cancer metastasis by enriching gut Parabacteroides distasonis
Journal Title: Journal of Advanced Research
DOI: 10.1016/j.jare.2024.11.024
IF: 11.4
PMID: 39571733

Abstract: The intricate interplay of interleukin-10 (IL-10) and gut microbiota influences tumor development and progression, yet the impacts on colorectal cancer (CRC) metastasis remain incompletely understood. The impact of Il10 deficiency on CRC metastasis was first evaluated in CRC metastasis tumor samples and mouse model. We revealed that serum IL-10 levels were markedly elevated in metastatic CRC patients compared to non-metastatic cases. In parallel, Il10-deficiency (Il10−/−) in mice resulted in decreased CRC metastasis in a gut microbiota-dependent manner. Mechanistically, Il10−/− mice reshaped gut microbiota composition, notably enriching P. distasonis. The enriched P. distasonis produced 4-HPAA, which activated the aryl hydrocarbon receptor (AHR) and subsequently inhibited the expression of VEGFA, a typical oncogene, thereby sequentially suppressing CRC metastasis. Importantly, engineered bacteria capable of producing 4-HPAA effectively hindered CRC metastasis. Furthermore, AHR depletion significantly disrupted the 4-HPAA-induced reduction in CRC cell migration and the inhibition of metastasis in both in vitro and in vivo lung metastasis mouse models. These findings demonstrate the significance of IL-10 deficiency in suppressing CRC metastasis through the 4-HPPA-AHR-VEGFA axis mediated by gut P. distasonis, suggesting that P. distasonis or 4-HPAA supplementation could offer a promising therapeutic strategy for CRC metastasis prevention.

Keywords: Colorectal cancer therapy, Metastasis, Interleukin-10, Parabacteroides distasonis

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Figure Source: J Adv Res. 2024 Nov 19:S2090-1232(24)00543-5. doi: 10.1016/j.jare.2024.11.024.